Case Report: Probable Myocarditis After Covid-19 mRNA Vaccine in a Patient With Arrhythmogenic Left Ventricular Cardiomyopathy

Arrhythmogenic left ventricular cardiomyopathy (ALVC) is a rare heritable heart-muscle disorder characterized by a progressive loss of left ventricular myocardium and its replacement by fibrofatty tissue. Myocarditis is an inflammatory disease of the heart that may occur secondary to infections, immune system activation or exposure to drugs. Hot phases of ALVC present with chest pain and troponin rise, mimicking acute viral myocarditis and indicate a progression of the disease. Recently, myocarditis has also been described as an infrequent complication of coronavirus disease 2019 (Covid-19) mRNA vaccines. We herein report for the first time a case of probable myocarditis induced by Covid-19 vaccine in a patient with previous medical history of ALVC. We aim to highlight the common characteristics of ALVC and Covid-19 vaccine myocarditis and work through the differential diagnosis of these two entities.

Cardiomyopathies: An Overview

Background: Cardiomyopathies are a heterogeneous group of pathologies characterized by structural and functional alterations of the heart. Aims: The purpose of this narrative review is to focus on the most important cardiomyopathies and their epidemiology, diagnosis, and management. Methods: Clinical trials were identified by Pubmed until 30 March 2021. The search keywords were “cardiomyopathies, sudden cardiac arrest, dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive cardiomyopathy, arrhythmogenic cardiomyopathy (ARCV), takotsubo syndrome”. Results: Hypertrophic cardiomyopathy (HCM) is the most common primary cardiomyopathy, with a prevalence of 1:500 persons. Dilated cardiomyopathy (DCM) has a prevalence of 1:2500 and is the leading indication for heart transplantation. Restrictive cardiomyopathy (RCM) is the least common of the major cardiomyopathies, representing 2% to 5% of cases. Arrhythmogenic cardiomyopathy (ARCV) is a pathology characterized by the substitution of the myocardium by fibrofatty tissue. Takotsubo cardiomyopathy is defined as an abrupt onset of left ventricular dysfunction in response to severe emotional or physiologic stress. Conclusion: In particular, it has been reported that HCM is the most important cause of sudden death on the athletic field in the United States. It is needless to say how important it is to know which changes in the heart due to physical activity are normal, and when they are pathological.

Risk Stratification in Arrhythmogenic Right Ventricular Cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC), also called arrhythmogenic right ventricular dysplasia or arrhythmogenic cardiomyopathy, is a genetic disease characterised by progressive myocyte loss with replacement by fibrofatty tissue. This structural change leads to the prominent features of ARVC of ventricular arrhythmia and increased risk for sudden cardiac death (SCD). Emphasis should be placed on determining and stratifying the patient’s risk of ventricular arrhythmia and SCD. ICDs should be used to treat the former and prevent the latter, but ICDs are not benign interventions. ICDs come with their own complications in this overall young population of patients. This article reviews the literature regarding the factors that contribute to the assessment of risk stratification in ARVC patients.

A challenging case of arrhythmogenic right ventricular cardiomyopathy presenting as fulminant myocarditis

ABSTRACT Arrhythmogenic right ventricular cardiomyopathy (ARVC) is known as a primary genetic heart disease that leading to the myocardial deposition of fibrofatty tissue in right ventricular (RV) wall. Sometimes, it occurs in the left ventricular (LV) subepicardial wall. This study introduces a child referred to our hospital with influenza-like symptoms and ventricular tachyarrhythmia, followed by cardiac failure. However, in our subsequent evaluation, there was evidence of severe LV and RV dysfunction based on the echocardiography. Moreover, cardiac magnetic resonance showed not only the major criteria of ARVC but also those of Lake Luise seen in myocarditis. Regarding the deteriorating condition during the hospital course, he was later scheduled for heart transplantation. Finally, the histopathological study of explanted heart revealed RV myocyte atrophy with the infiltration of fibrofatty tissue in myocardium diagnostic of ARVC, resolving dilemma between ARVC and myocarditis.

Use of pedicled dartos flap wrap around technique in elaborarted perineal repair of complex pelvic fracture urethral distraction defect

Objectives: To describe the use of a pedicled dartos flap between the pubic bone and bulbar urethra after elaborate perineal urethroplasty in complex pelvic fracture urethral distraction defect. This is to prevent the risk of entrapment of the anastomotic area within a fibrous scar and hence prevent the risk of urethral stricture recurrence. Our objective is also to theorise the entity of bulbar urethral entrapment to describe the trapping of the bulbar urethra by fibrosis after extensive bone resection in complex cases of pelvic fracture urethral distraction defect. Methods: Ten patients with complex pelvic fracture urethral distraction defect underwent perineal urethroplasty at our institution from 2017 to 2019. Urethroplasty was done using the elaborated perineal approach in the standard fashion. Pedicled fibrofatty tissue along with dartos from the scrotum was used to separate the site of urethral anastomosis from the bare pubic bone and fill the dead space. Results: All patients are asymptomatic with no stricture recurrence in follow-up. Conclusions: Vascularised pedicle flap should become an important tenant in the elaborated perineal repair of complex pelvic fracture urethral distraction defect. It provides an ideal option in this scenario by decreasing the risk of urethral stricture recurrence without adding morbidity and minimum extra operative time. Level of evidence: Not applicable.

Arrhythmogenic cardiomyopathy: pathogenesis, pro-arrhythmic remodelling, and novel approaches for risk stratification and therapy

Arrhythmogenic cardiomyopathy (ACM) is a life-threatening cardiac disease caused by mutations in genes predominantly encoding for desmosomal proteins that lead to alterations in the molecular composition of the intercalated disc. ACM is characterized by progressive replacement of cardiomyocytes by fibrofatty tissue, ventricular dilatation, cardiac dysfunction, and heart failure but mostly dominated by the occurrence of life-threatening arrhythmias and sudden cardiac death (SCD). As SCD appears mostly in apparently healthy young individuals, there is a demand for better risk stratification of suspected ACM mutation carriers. Moreover, disease severity, progression, and outcome are highly variable in patients with ACM. In this review, we discuss the aetiology of ACM with a focus on pro-arrhythmic disease mechanisms in the early concealed phase of the disease. We summarize potential new biomarkers which might be useful for risk stratification and prediction of disease course. Finally, we explore novel therapeutic strategies to prevent arrhythmias and SCD in the early stages of ACM.

Ultrasound-guided TriVex™-powered phlebectomy for debulking of peripheral vascular anomalies – A novel treatment technique

Background Large vascular anomalies on the trunk or limbs are rare and prove challenging to treat. Currently, treatment options include conservative management, embolisation, sclerotherapy or surgical excision. Once the lesion has been embolised, or if it spontaneously involutes, the residual fibrofatty tissue may be painful and require debulking. Surgical debulking may be associated with complicated wound healing, infection, scarring and may not be not feasible for large lesions. Method We present our technique of using TriVex™-powered phlebectomy to debulk vascular anomalies. Our modification involved performing sclero-emobolisation on the target lesion first to mitigate the risk of haematoma formation. We also used ultrasound guidance to increase the precision and eliminate the use of TriVex™ illuminator. Results Excellent symptom relief and cosmetic outcome were achieved in three patients treated using this method. Conclusion We believe the novel technique of ultrasound-guided TriVex™-powered system provides a viable alternative to surgical debulking of large or complex vascular anomalies.

Neural substrate for atrial fibrillation: implications for targeted parasympathetic blockade in the posterior left atrium

The parasympathetic (P) nervous system is thought to contribute significantly to focal atrial fibrillation (AF). Thus we hypothesized that P nerve fibers [and related muscarinic (M2) receptors] are preferentially located in the posterior left atrium (PLA) and that selective cholinergic blockade in the PLA can be successfully performed to alter vagal AF substrate. The PLA, pulmonary veins (PVs), and left atrial appendage (LAA) from six dogs were immunostained for sympathetic (S) nerves, P nerves, and M2 receptors. Epicardial electrophysiological mapping was performed in seven additional dogs. The PLA was the most richly innervated, with nerve bundles containing P and S fibers (0.9 ± 1, 3.2 ± 2.5, and 0.17 ± 0.3/cm2 in the PV, PLA, and LAA, respectively, P < 0.001); nerve bundles were located in fibrofatty tissue as well as in surrounding myocardium. P fibers predominated over S fibers within bundles (P-to-S ratio = 4.4, 7.2, and 5.8 in PV, PLA, and LAA, respectively). M2 distribution was also most pronounced in the PLA (17.8 ± 8.3, 14.3 ± 7.3, and 14.5 ± 8 M2-stained cells/cm2 in the PLA, PV, and LAA, respectively, P = 0.012). Left cervical vagal stimulation (VS) caused significant effective refractory period shortening in all regions, with easily inducible AF. Topical application of 1% tropicamide to the PLA significantly attenuated VS-induced effective refractory period shortening in the PLA, PV, and LAA and decreased AF inducibility by 92% ( P < 0.001). We conclude that 1) P fibers and M2 receptors are preferentially located in the PLA, suggesting an important role for this region in creation of vagal AF substrate and 2) targeted P blockade in the PLA is feasible and results in attenuation of vagal responses in the entire left atrium and, consequently, a change in AF substrate.